• J Trauma · Aug 2002

    Granulocyte colony-stimulating factor: release is not impaired after burn wound infection.

    • Richard Gamelli, Li-Ke He, and Elisabeth Hahn.
    • Department of Surgery, Loyola University Medical Center, Burn & Shock-Trauma Institute, Maywood, Illinois 60153, USA. rgamell@wpo.it.luc.edu
    • J Trauma. 2002 Aug 1;53(2):284-9; discussion 289-90.

    BackgroundThe production of granulocyte colony-stimulating factor (G-CSF), the lineage specific essential regulator of neutrophil progenitor cell proliferation and differentiation, has been thought to be impaired in the setting of burn infection. The ability to directly measure murine G-CSF allows the further delineation of the G-CSF response in a clinically relevant model of thermal injury and infection.MethodsWe used a commercially available solid phase enzyme-linked immunoabsorbent assay to quantify G-CSF production after burn wound infection in mice. Bone marrow cells, splenic cells, and serum were obtained from BDF1 mice on day 3 after a 15% total body surface area full-thickness scald burn with or without Pseudomonas aeruginosa burn wound infection. G-CSF production of bone marrow cells or splenic cells and the serum level of G-CSF were measured. A clonogenic assay of bone marrow and spleen granulocyte-macrophage progenitor cells as well as blood leukocyte counts were also performed.ResultsAfter burn sepsis, we noted that G-CSF production of the bone marrow and spleen was significantly increased; the numbers of progenitor cells in bone marrow and spleen were markedly enhanced; serum values of G-CSF were 14 times greater than control values; serum colony-stimulating activity was greater than in control mice; and total blood leukocyte counts were significantly depressed.ConclusionThese findings support the notion that granulocytopoietic failure after burn sepsis is not significantly related to defective endogenous G-CSF synthesis. More likely, hyporesponsiveness of granulocyte progenitor cells to G-CSF, changes in the relative balance of granulocyte versus monocyte progenitors within the granulocyte-macrophage progenitor cell compartment, and enhanced release of monocyte lineage specific growth factors are the critical elements responsible for burn infection-induced hematopoietic failure.

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